ADH circulates in the blood to the distal tubule and collecting ducts of individual kidney nephrons. Here, it binds to a basement membrane receptor, termed V2, causing a rise in intracellular secondary messengers (cAMP). This triggers:
Cytoskeletal microtubules are involved in the formation of new new membrane channels. Overall, there is an increase in the passive reabsorption of water and active reabsorption of sodium.
Clinically, this explains why anti-prostaglandins e.g. indomethacin promote ADH activity while the reverse is found with drugs that hinder microtubular function e.g. colchicine. By contrast, less is known about the way lithium carbonate and demeclocycline work: both oppose ADH action on the kidney and are used to treat states of hypersecretion.
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